Inter-individual variability in sensory weighting of a plantar pressure-based, tongue-placed tactile biofeedback for controlling posture

The purpose of the present experiment was to investigate whether the sensory weighting of a plantar pressure-based, tongue-placed tactile biofeedback for controlling posture could be subject to inter-individual variability. To achieve this goal, 60 young healthy adults were asked to stand as immobile as possible with their eyes closed in two conditions of No-biofeedback and Biofeedback. Centre of foot pressure (CoP) displacements were recorded using a force platform. Overall, results showed reduced CoP displacements in the Biofeedback relative to the No-biofeedback condition, evidencing the ability of the central nervous system to efficiently integrate an artificial plantar-based, tongue-placed tactile biofeedback for controlling posture during quiet standing. Results further showed a significant positive correlation between the CoP displacements measured in the No-biofeedback condition and the decrease in the CoP displacements induced by the use of the biofeedback. In other words, the degree of postural stabilization appeared to depend on each subject's balance control capabilities, the biofeedback yielding a greater stabilizing effect in subjects exhibiting the largest CoP displacements when standing in the No-biofeedback condition. On the whole, by evidencing a significant inter-individual variability in sensory weighting of an additional tactile information related to foot sole pressure distribution for controlling posture, the present findings underscore the need and the necessity to address the issue of inter-individual variability in the field of neuroscience.     

Protective effect of bromelain on corrosive burn in rats

IntroductionIn some cases, the tongue and oesophagus tissues are damaged by the corrosive burn. Surgical interventions may cause scar formation, and severe burns treatment methods are limited. This study aims to investigate bromelain, a phytotherapeutic product, on the corrosive burn as a non-surgical option and as an adjunctive therapy, insofar as the treatment of corrosive wounds is not limited only to the treatment of oxidative stress and inflammatory reactions.MethodsOn the tongues of Wistar albino rats, chemically produced oral ulcers were created by topical application of NaOH (40%) solution, and in the distal oesophagus same mixture was applied to produce a corrosive oesophageal burn. For a week, they were treated orally by bromelain (100 mg/kg/day) or saline solution. At the end of seven days, animals were decapitated to remove the tongue and oesophagus, and blood samples were collected to obtain serum. Myeloperoxidase (MPO) activity, malondialdehyde (MDA), glutathione (GSH), interleukin-1 beta (IL-1β) and tumour necrosis factor-alpha (TNF-α) concentrations were measured in serum, and luminol and lucigenin chemiluminescence (CL) were measured in tissue samples.ResultsMDA and CL values were significantly increased, and GSH levels in tissue significantly decreased due to the corrosive burns. Saline treated corrosive burn group measured higher in the serum cytokines in according to the control group.ConclusionsBromelain administration decreased oxidant and inflammatory parameters and increased antioxidant levels in NaOH-induced corrosive burns. Thus, we concluded that bromelain may protect the tongue and oesophagus tissues with its anti-inflammatory and antioxidant effects.     

模拟失重及高+Gx对猴舌横纹肌细胞结构及HSP70表达的影响

目的探讨模拟失重及高+Gx对猴舌横纹肌组织结构和热休克蛋白70(heat shock protein 70,HSP70)表达的影响。方法 12只雄性猕猴随机分为4组,正常对照组(A)、30d模拟失重组(B),+13Gx/230s组(C)、30d模拟失重后超重组(D),其中D组根据过载峰值又分为+11Gx/270s(D1)、+13Gx/230s(D2)和+15Gx/200s(D3)。动物放血处死后取材,采用组织病理学和免疫组化的方法,观察猴舌横纹肌组织结构及HSP70的表达情况。结果 A组可见正常的舌横纹肌结构,其他组舌横纹肌细胞结构基本正常,偶见细胞间质稀疏,细胞排列紊乱以及横纹不清或消失。A组舌横纹肌细胞HSP70呈阴性表达,细胞核与细胞浆均无明显着色;B组、C组和D组舌横纹肌细胞胞核与胞浆均着色明显,呈阳性表达,较A组变化显著。HSP70免疫组化积分显示,D组比B组和C组变化显著(P<0.05),但D1、D2、D3无明显差别(P>0.05)。结论 30d模拟失重和高+13Gx/230s均可使猴舌横纹肌细胞产生应激反应,引起HSP70的表达增强,并可能伴有损伤。模拟失重与过载超重具有协同作用,两者可能加重了对舌横纹肌的影响。     

应用蛋白质芯片技术筛选人舌鳞癌细胞株差异性炎症因子的初步研究

目的研究应用蛋白质芯片(抗体芯片)技术筛选、分析人舌鳞状细胞癌细胞株中差异性炎症因子的效果,为进一步探讨口腔癌与炎症的关系奠定基础。方法体外培养人舌鳞癌细胞株UM-1、CAL-27、Tca-8113和人正常口腔黏膜上皮细胞,消化后分别提取胞内、胞外蛋白,上芯片孵育,封闭,清洗。采用激光扫描仪扫描芯片,Axon GenePix Pro6.0软件提取芯片数据,对获得的80种炎症因子表达数据采用AAH-CYT-G5软件分析,上调因子信号值以大于200、比值大于2.0为纳入标准;下调因子信号值以大于200、比值小于0.66为纳入标准,分别对3种人舌鳞癌细胞株(UM-1、CAL-27、Tca-8113)与人正常口腔黏膜上皮细胞,以及高侵袭性细胞株(UM-1、CAL-27)与低侵袭性细胞株(Tca-8113)进行两两比较,筛选出差异性炎症因子。挑选3种显著差异性炎症因子,用酶联免疫吸附法再次检测其蛋白表达,所得结果用单因素方差分析进行统计学分析,进一步验证芯片法所获得的结果。结果根据纳入标准,从检测的80种因子中筛选出有表达的炎症因子9个,包括干扰素诱导蛋白10(inter-feron inducible protein10,IP-10)、巨噬细胞炎症蛋白-1β(macrophage inflammatory protein1β,MIP-1β)、巨噬细胞炎症蛋白-3α(macrophage inflammatory protein-3α,MIP-3α)、骨保护素蛋白(osteoprotegerin,OPG)、调节活化蛋白(regulated upon activation normal T-cell expressed and secreted,RANTES)、白细胞介素1β(interleukin1β,IL-1β)6种舌鳞癌细胞株中高表达的细胞因子,及单核细胞趋化因子4(monocyte chemoattractant protein4,MCP-4)、胰岛素样生长因子结合蛋白4(insulin-like growth factor binding protein-4,IGFBP-4)、转化生长因子-β3(transforminggrowth factor-β3,TGF-β3)3种舌鳞癌细胞株中低表达的细胞因子。鳞状细胞癌细胞和正常口腔鳞状上皮细胞之间比较,胞内IL-1β呈高表达,MCP-4呈低表达,胞外OPG呈高表达;高、低侵袭性细胞株之间比较,胞内RANTES呈高表达,IGFBP-4、TGF-β3呈低表达,胞外IP-10、MIP-1β、MIP-3α呈高表达。酶联免疫吸附法检测发现UM-1和CAL-27胞外IP-10、MIP-1β、MIP-3α的表达量和Tca-8113相比呈高表达,差异有统计学意义(P<0.05)。其结果与芯片筛选结果一致。结论蛋白质芯片技术能够较为准确地筛选出不同舌鳞癌细胞株之间差异性炎症因子,这些差异性炎症因子可能与肿瘤细胞的生物学行为有一定的联系。     

兔舌癌哨位淋巴结微转移模型的建立

目的:建立兔舌癌哨位淋巴结(sentinel lymph node,SLN)微转移模型,为进一步研究舌癌区域淋巴结转移的发生、发展机制及防治提供实验平台。方法:先正位、多循环移植Vx-2癌瘤于兔舌,每次8只兔,筛选出高淋巴转移潜力移植瘤;再将其移植到40只兔的舌部,分别于移植后第8、10、12、14和16天各随机处死8只,取出兔舌Vx-2移植瘤SLN,经连续切片和免疫组织化学检测其微转移形成情况。应用SPSS 17.0软件包对结果进行统计学分析。结果:经3次正位循环移植后,所得Vx-2移植瘤舌移植后SLN转移率达100%(8/8);该高淋巴转移潜力移植瘤移植兔舌后10~12 d,所获移植瘤SLN微转移发生率为100%(8/8)。结论:应用本研究筛选的高淋巴转移潜力Vx-2瘤移植兔舌后10~12 d,可获得较稳定的兔舌癌SLN微转移模型。     

芪蓝颗粒对SD大鼠舌黏膜癌变过程中EGFR变化的影响

目的：探讨中药芪蓝颗粒阻癌抑癌的作用机制。方法：SD大鼠150只,随机分为A、B、C、D、E共5组,A、B、C、D组用0.002%4NQO制备大鼠舌癌变模型,其中B、C、D组在制备模型的同时,用不同剂量芪蓝颗粒进行干预,A组为模型对照组,E组为正常对照组。各组于中药干预的9、18、27、36周时分别处死7只动物,取舌组织光镜下观察其病理变化,采用免疫组化技术检测各组表皮生长因子受体（EGFR）的表达。结果：A组总体癌变率39.29%,明显高于B、C、D组（P〈0.05）。A组中EGFR的表达从正常口腔黏膜→各级异型增生→癌变,其阳性表达率呈递增趋势,差异有统计学意义（P〈0.01）。在大鼠异常增生舌组织中A组的EGFR阳性表达率为6/11明显高于B、C、D组,差异有统计学意义（P〈0.05）。在大鼠舌癌组织中进行中药干预组EGFR的阳性表达明显低于A组（P〈0.05）,差异有统计学意义（P〈0.05）。E组EGFR蛋白表达均为阴性。结论：芪蓝颗粒具有明显的抑癌阻癌效果,它可能通过下调细胞中EGFR的表达水平,起到抑癌阻癌的作用。     

短发夹RNA干扰血管内皮生长因子对舌癌耐药细胞移植瘤的影响

目的 研究短发夹RNA(short hairpin RNA,shRNA)干扰血管内皮生长因子(vascular endothelial growth factor,VEGF)的表达对人舌癌耐药细胞Tca-顺铂(Cisplatin,DDP)移植瘤的影响及可能机制.方法 以人舌癌Tca8113细胞系为亲本诱导建立耐药Tca-DDP细胞系,将其接种于裸鼠背侧皮下,建立移植瘤模型.模型动物分为4组,即空白对照组(非转染)、空载体组(转染空质粒载体)、无关片段组(转染无关对照质粒)、干扰质粒组(转染靶向VEGF的shRNA表达载体),每组6只,每3天以脂质体为载体作瘤体内及瘤周多点注射.观测移植瘤生长曲线,转染l0次后取瘤体称重,免疫组化法检测移植瘤微血管密度,原位杂交法检测移植瘤VEGFmRNA,免疫组化技术检测移植瘤VEGF、多药耐药蛋白P糖蛋白(P-glycoprotein,P-gp)、B细胞淋巴瘤-白血病因子2(B cell lymphoma/leukemia-2,bcl-2)及胞外信号调节激酶2蛋白(extracellular signal-regulated kinase 2,ERK-2).结果 干扰质粒组的瘤体生长明显受到抑制(P＜0.05),移植瘤重量(0.4781±0.0860)g及微血管密度(7.35±1.31)个/视野,低于其他3组(P＜0.05),且VEGF的mRNA及蛋白、P-gp、bcl-2及ERK-2的相对表达量分别为(0.0767±0.0234)、(0.1301±0.0433)、(0.1517±0.0184)、(0.1218±0.0251)及(0.1178±0.0291),表达均显著减少(P＜0.05).结论 RNA干扰抑制VEGF的表达,可抑制人舌癌Tca8113耐药细胞移植瘤的生长及血管生成,下调P-gp、bcl-2及ERK-2表达水平,提示靶向抑制VEGF可能是治疗耐药舌癌途径之一.

Abstract：

Objective To study the in vivo interference effects of vascular endothelial growth factor (VEGF) short hairpin RNA (shRNA) on xenografts of drug-resistant tongue cancer cells. Methods Drugresistant tongue caner cells Tca/Cisplatin(DDP) were injected subcutaneously into nude mice to establish xenograft models, which were randomly divided into non-transfected group, mock control group, control group transfected with scrambled sequence plasmid, interference group transfected with VEGF-shRNA expression plasmid. Liposome-mediated plasmid transfection was done in the latter three groups every three days. Xenografts were observed and tumor growth curve was measured. After the 10th transfection, tumors were anatomized and weigh. Microvessel density was detected by immunohistochemical staining. In situhybridization assay was used to test VEGF mRNA, and immunohistochemistry to test VEGF, P-glycoprotein ( P-gp), B cell lymphoma/leukemia-2 ( bcl-2 ) and extracellular signal-regultaed kinase 2 (ERK-2) protein. Results Tumor growth in VEGF-shRNA interference group was significantly slow. Tumor weight was (0.4781 ±0.0860) g, microvessel density (7.35 ± 1.31)/view, VEGF mRNA(0.0767 ±0.0234), VEGF protein (0.1301 ± 0.0433 ), P-gp (0.1517 ± 0.0184 ), bcl-2 ( 0.1218 ± 0.0251 ) and ERK-2 protein (0.1178 ±0.0291 ) in VEGF-shRNA interference group; all of them were less than those in the other three groups( P ＜ 0.05 ). Conclusions Inhibition targeting VEGF may become a potential therapy for drugresistant tongue cancer.     

反义微小RNA-21寡核苷酸抑制Tb3.1人舌鳞状细胞癌增殖的体外研究

目的 探讨反义微小RNA-21寡核苷酸(antisense oligonucleotide micro RNA-21,AS-miRNA-21)抑制Tb3.1人舌鳞状细胞癌增殖的效果和机制.方法 实验分3组,①空白对照组;②无义寡核苷酸转染组;③AS-miRNA-21转染组.寡核苷酸介导转染反义寡核苷酸敲低Tb3.1细胞miRNA-21表达.使用荧光实时定量聚合酶链反应(PCR)鉴定转染后Tb 3.1细胞miRNA-21表达水平;甲基噻唑基四唑(MTT)法检测转染后Tb 3.1细胞生存率;流式细胞术检测转染后Tb3.1早期凋亡;Matrigel基质生长实验检测转染后Tb 3.1细胞生长形成球形集落能力;Transwell体外迁移实验检测转染后Tb 3.1细胞迁移能力;蛋白质印迹法检测转染后Tb3.1细胞增殖核抗原(antigen KI-.67,Ki67)、B细胞淋巴瘤2(B cell lymphoma 2,Bcl-2)、人第10号染色体缺失的磷酸酶及张力蛋白同源的基因(phosphatase and tensin homolog,PTEN)、基质金属蛋白酶2、9(matrix metalloproteinase 2/9,MMP-2、MMP-9)和组织基质蛋白酶抑制因子蛋白1(tissue inhibitor of metalloproteinase 1,TIMP-1)蛋白表达.结果 荧光实时定量PCR显示转染后miRNA-21表达水平下调;转染第4天,AS-miRNA-21转染组肿瘤细胞生长速度[(53.43±11.83)%]低于其他两组[(91.32±8.02)%和100%](F=27.02,P=0.00);细胞凋亡率显著升高[(12.23±2.92)%,F=26.641,P=0.001];AS-miRNA-21转染组细胞生长不能形成球形克隆且通过Transwell小室聚碳酸酯膜的细胞数小于空白对照组(F=268.231,P=0.000);Ki67、Bcl-2、MMP-2和MMP-9蛋白表达下调,PTEN和TIMP-1蛋白表达上调.结论 敲低miRNA-21后Tb3.1人舌癌细胞增殖与侵袭能力被抑制,并为探索miRNA-21调控人舌癌发生机制提供实验依据.

Abstract：

Objective To investigate the effect of micro RNA-21 (miRNA-21) knocking on the Tb3.1 human tongue squamous cell carcinoma growth. Methods Anti-sense miRNA-21 oligonucleotide was delivered with oligofectamine to suppress Tb 3. 1 tongue cancer cell growth in vitro. Real-time polymerase chain reaction (PCR) was conducted to detect the miRNA-21 expression after transfection. Methyl thiazolyl tetrazolium(MTT) assay was used to determine Tb 3. 1 cell survival rate. Apoptosis were examined by flowcytometry. Matrigel matrix and transwell assay were used to determine Tb 3.1 cell colony formation and migration ability. Antigen KI-67 (Ki67), B cell lymphoma (Bcl-2), phosphatase and tensin homolog (PTEN), matrirx metalloproteinase 2(MMP-2, MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1) protein expression in Tb 3. 1 cell were measured by Western blotting. Results miRNA-21 expression was decreased in miRNA-21 antisense oligonucleotide (ASODN) group. The survival rate of Tb 3. 1 cells with AS-miRNA-21 transfection was significantly suppressed (F=27.02, P = 0.00) and early phase apoptosis(F =26. 641 ,P = 0. 001) induced in Tb 3.1 cell. Ki67, Bcl-2, MMP-2 and MMP-9 protein weredown regulated while PTEN and TIMP-1 protein expression was increased. Conclusions Blocking miRNA-21 expression in Tb3.1 cell could suppress cancer cell growth in vitro and miRNA-21 can serve as a novel target candidate for human tongue cancer gene therapy.     

ERK及nm23-H1蛋白表达与舌癌侵袭、转移的关系

目的:探讨ERK及nm23-H1在舌癌中的表达及与侵袭、转移的关系。方法:采用免疫组织化学方法检测ERK及nm23-H1在74例舌癌中的表达。采用SPSS10.0软件包对数据进行统计学处理。结果:ERK的表达与临床分期及颈淋巴结转移呈正相关。nm23-H1的表达与临床分期及颈淋巴结转移呈负相关。ERK表达与nm23-H1表达呈负相关。ERK阳性同时nm23-H1阴性表达者,颈淋巴结转移率显著高于ERK阴性同时nm23-H1阳性表达者,舌癌中ERK及nm23-H1的表达率呈负相关。结论:ERK及nm23-H1的表达与舌癌的侵袭及颈淋巴结转移密切相关,联合检测具有一定的临床意义,有望成为判断侵袭、转移的指标之一。     

干扰素γ对舌鳞癌细胞增殖影响的研究

目的：观察干扰素γ对舌鳞癌细胞增殖的影响。方法：采用不同浓度的干扰素γ对舌鳞癌细胞处理,观察肿瘤细胞的增殖情况;基因芯片分析干扰素γ处理后基因表达的变化,并采用实时定量PCR验证;western blot检测AKT信号通路的表达情况。结果：采用不同浓度的干扰素γ处理CAL27细胞后,肿瘤细胞的生长明显加快,肿瘤生长72、96h后,细胞数量有显著性差异（P〈0.05）。基因芯片结果显示PIK3C2A的表达提高2.5倍以上。western blot结果证实干扰素γ处理细胞后,AKT信号通路被激活。结论：干扰素γ处理舌鳞癌细胞后能加快肿瘤细胞的生长,激活AKT信号通路,其不适用直接对舌鳞癌进行治疗。